HDAC3 and cancer: The heterozygous mutation of mouse ANKRD11 caused a decreased cortical precursor proliferation and perturbed genesis of neurons, leading to the increase of HDAC3‐regulated H4K5ac, H4K8ac, H3K9ac, and H4K16ac.[24a] The phenotype of biallelic 65K/RNPC3 variants is mainly associated with growth hormone deficiency, delayed bone, intellectual disability, and brain anomalies.[44] We also searched human cancer data (GEPIA2 database), and found that the expression of Hs65K, HsANKRD11, and HDAC3 is significantly changed in tumors versus normal tissues (Figure S8E, Supporting Information).